Saudi Journal of Kidney Diseases and Transplantation

: 2013  |  Volume : 24  |  Issue : 6  |  Page : 1262--1264

Celiac disease a rare cause of nephrogenic ascites

Jwaher Al-bderat, Issa Hazza, Rana Haddad 
 Pediatric Department, Queen Rania Alabdullah Hospital of Pediatrics, King Hussein Center, Amman, Jordan

Correspondence Address:
Issa Hazza
Pediatric Department, Queen Rania Alabdullah Hospital of Pediatrics, King Hussein Center, Amman

How to cite this article:
Al-bderat J, Hazza I, Haddad R. Celiac disease a rare cause of nephrogenic ascites.Saudi J Kidney Dis Transpl 2013;24:1262-1264

How to cite this URL:
Al-bderat J, Hazza I, Haddad R. Celiac disease a rare cause of nephrogenic ascites. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2021 Apr 16 ];24:1262-1264
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Full Text

To the Editor,

Celiac disease (CD), also known as gluten- sensitive enteropathy or non-tropical sprue, is caused by sensitivity to dietary gluten and related proteins in genetically sensitive individuals. It is an immune-mediated enteropathy that is associated with a variety of autoimmune diseases such as type-1 diabetes mellitus, autoimmune thyroid disorders and Sjogren's syndrome. [1] However, CD and kidney disease have been reported only rarely in the same individual, although it is sometimes listed as one of the associated diseases of IgA nephropathy. The symptoms of CD are diverse, and may be absent or very subtle. [2],[3] We present here a rare case of a post-renal transplant patient who was diagnosed as CD when she presented as a case of refractory ascites.

A 12-year-old girl with steroid-resistant nephrotic syndrome due to biopsy-proven focal segmental glomerulosclerosis (FSGS) since the age of 3 years developed end-stage renal failure at the age of 10 years and was started on hemodialysis. She developed significant ascites and her dialysis sessions were frequently complicated by hypotensive episodes. The etiological work-up did not reveal any obvious cause and she was initially considered to have nephrogenic ascites. Her weight was 29 kg and she had massive ascites with an abdominal circumference of 76 cm and pitting edema of both lower extremities. Laboratory results showed packed cell volume (PCV) as 30.3% and mean corpuscular volume (MCV) as 78 fL. Serum albumin was 11 gm/L and total protein 54 gm/L and liver enzymes and the lipid profile were normal. The thyroid function test was also normal. Cardiac evaluation showed a good bilateral ventricular function. Hepatic Doppler ultrasound showed an enlarged liver (15 cm) with normal homogeneous echogenicity. The inferior vena cava was patent and the main hepatic veins and portal vein had normal blood flow. An abdominal computed tomography angiogram showed no thrombosis. Ascitic fluid albumin and WBC count were 27 gm/L and 48 cells/cm 3 , respectively, with negative cytological, bacteriologic and mycobacterial examination. After 5 months on dialysis, she underwent successful living related kidney transplant and was maintained on tacrolimus, mycophenolate and prednisolone. Her baseline creatinine on discharge post-transplant was 0.7 mg/dL. The patient continued to have increasing abdominal girth due to ascites, for which she needed recurrent admissions for abdominal tapping along with human albumin infusion. Each time upon her admission she had a rise in her serum creatinine that returned to normal after tapping and human albumin administration. On her last admission to our center, the patient presented with frequent diarrhea and anorexia along with increasing ascites; therefore, she was shifted from mycophenolate to azathioprine with no relief in her symptoms. Hence, upper gastro-endoscopy (UGE) and colonoscopy with small bowel biopsy were performed, which revealed villous atrophy with intraepithelial lymphocytic infiltrate, accompanied by crypt hyperplasia consistent with CD [Figure 1] and anti- transglutaminase antibody was also reported to be positive. Therefore, a gluten free diet was started and, dramatically, all her symptoms and signs improved, including ascites. Her present weight is 26 kg and she now has an abdominal circumference of 67 cm, with normal serum creatinine.{Figure 1}

The true incidence of CD and chronic kidney disease has not been established. [4] It was suggested that immune characteristics associated with CD increase the risk of chronic kidney disease and moderately increase the risk of any form of glomerulonephritis. [5] Gimenez et al [6] reported five cases of nephrotic syndrome in children associated with CD. A few cases of CD associated with membranous nephropathy in adults have also been reported. [7],[8],[9] Our case had FSGS as the primary disease and, to the best of our knowledge, an association of CD with FSGS has never been reported in children earlier. A Medline search revealed only one case of an 83-year-old woman who had FSGS-associated polycythemia and CD. [10] The presence of massive ascites in our case, which was resistant to dialysis and accompanied by frequent hypotensive episodes, raised the suspicion of nephrogenic ascites, which is an entity that manifests itself as refractory ascites in patients with end-stage renal failure where portal hypertension, infection and malignant process per se have been excluded. Most of these patients are undergoing hemodialysis. [11] Patients frequently present with hypertension, moderate to massive ascites, ankle edema, cachexia and history of dialysis-associated hypotension. [12] Gluckze et al [13] had reported that continuous ambulatory peritoneal dialysis, peritono-venous shunt and renal transplantation appear to be effective in controlling ascites formation in nephrogenic ascites, which was not the case with our patient, who continued to have persistent ascites even after successful transplant, making our initial diagnosis unlikely. However, the result of small bowel biopsy consistent with CD along with a positive serological test for trans-glutaminase antibodies strengthened the diagnosis of CD, in addition to the dramatic improvement on gluten-free diet regarding her symptoms and ascites. A possibility of CD as a cause for resistant ascitis in dialysis patients should also be considered before labeling it as neprogenic ascites.


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